Respiratory Changes in Thromboembolic Disease

Nikodýmová, L; Daum, S; Stiksa, J; Widimský, Jiří

doi:10.1159/000192552

Cited by 9 publications

(3 citation statements)

References 11 publications

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“…Use of the etCO2 to estimate the alveolar dead space fraction as opposed to the mixed-expired CO2 was chosen because the end-tidal equation provides a more specific estimate of the alveolar dead space fraction compared with the physiological dead space fraction, which measures both airway and alveolar dead space (25). VD/VTalv correlates with pulmonary vascular resistance (22), and perfusion defects in humans with PE (17) decreases in parallel with reduction in perfusion defects during treatment (25) and correlates with the plasma concentration of TxB2 in dogs with PE (39).…”

Section: Methodsmentioning

confidence: 99%

Inhibition of prostaglandin synthesis during polystyrene microsphere-induced pulmonary embolism in the rat

Jones

Watts

Debelak

et al. 2003

American Journal of Physiology-Lung Cellular and Molecular Phys

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2002.-Our objective was to test the effect of inhibition of thromboxane synthase versus inhibition of cyclooxygenase (COX)-1/2 on pulmonary gas exchange and heart function during simulated pulmonary embolism (PE) in the rat. PE was induced in rats via intrajugular injection of polystyrene microspheres (25 m). Rats were randomized to one of three posttreatments: 1) placebo (saline), 2) thromboxane synthase inhibition (furegrelate sodium), or 3) COX-1/2 inhibition (ketorolac tromethamine). Control rats received no PE. Compared with controls, placebo rats had increased thromboxane B2 (TxB2) in bronchoalveolar lavage fluid and increased urinary dinor TxB2. Furegrelate and ketorolac treatments reduced TxB2 and dinor TxB2 to control levels or lower. Both treatments significantly decreased the alveolar dead space fraction, but neither treatment altered arterial oxygenation compared with placebo. Ketorolac increased in vivo mean arterial pressure and ex vivo left ventricular pressure (LVP) and right ventricular pressure (RVP). Furegrelate improved RVP but not LVP. Experimental PE increased lung and systemic production of TxB 2. Inhibition at the COX-1/2 enzyme was equally as effective as inhibition of thromboxane synthase at reducing alveolar dead space and improving heart function after PE. thromboembolism/treatment; cyclooxygenase; thromboxane; leukotriene; ketorolac; heart failure; Langendorff; animal model PULMONARY EMBOLISM (PE) continues to be a major cause of morbidity and mortality in the United States. In one large autopsy-based study, massive PE was the second leading cause of sudden death in adults aged Ͻ65 yr (4). The primary treatment strategy for massive PE is the recanalization of occluded pulmonary vasculature by fibrinolytic agents (11), catheter fragmentation (32), or surgical removal of clot (16). However, up to one-half of patients with massive PE have contraindications to fibrinolysis (15), and few hospitals have facilities for invasive treatment of PE. Even under optimal conditions (e.g., immediate bolus infusion of a fibrinolytic agent), these interventions require Ͼ2 h to effect a significant reduction in pulmonary vascular resistance (20). PE may also cause pulmonary vasoconstriction through the liberation of vasoconstrictive agents, including PGF 2␣ and thromboxane (Tx) A 2 and B 2 (10). PE can cause hypoxemia and increased pulmonary arterial pressure in previously healthy patients (19). Both hypoxemia and increased shear forces in the pulmonary vascular bed have been found to increase expression of the cyclooxygenase (COX)-2 gene (3). In humans with PE, blood concentrations of thromboxane have been found to be elevated for up to 7 days after onset of symptoms (10). Both the mechanical vascular occlusion and release of vasoconstrictive agents from massive PE appear to produce a synergistic effect that causes acute pulmonary hypertension, worsened gas exchange, impaired right ventricular (RV) function that can culminate in acute cor pulmonale, circulatory shock, and even death (26,30,39).In the ...

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Section: Methodsmentioning

confidence: 99%

Inhibition of prostaglandin synthesis during polystyrene microsphere-induced pulmonary embolism in the rat

Jones

Watts

Debelak

et al. 2003

American Journal of Physiology-Lung Cellular and Molecular Phys

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“…However, some authors confirmed the clinical value of the alveolo-arterial gradient of Pco2 for the diagnosis of thromboembolic disease (Llamas and Swenson, 1965;Mostyn and Luft, 1967;Nutter and Massumi, 1966;Robin et al, 1959Robin et al, , 1960. Other authors (Jones and Goodwin, 1965;Nikodymova, Daum, Stiksa, and Widimsky, 1968) measured the alveolo-arterial gradient of Pco2 in order to study the late sequels of pulmonary embolism; the mean alveolo-arterial gradient of Pco2 was not clearly abnormal but was, however, a little higher than in normal subjects. Nadel, Gold, and Burgess (1968) studied eight patients with dyspnoea due to obliteration of peripheral branches of the pulmonary artery; six of the eight cases had an abnormal alveolo-arterial gradient of Pco0.…”

Section: Methodsmentioning

confidence: 83%

Value of measurement of alveolo-arterial gradient of PCO2 compared to pulmonary scan in diagnosis of thromboembolic pulmonary disease

Vereerstraeten

Schoutens

Tombroff

et al. 1973

Thorax

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“…20 Additionally, V e increases. 34,35 The increased rate of ventilation may reflect a compensation for the increased percentage of each breath that is wasted on underperfused alveoli. PE, on the other hand, minimally affects, or decreases, airway dead space secondary to hypocarbic bronchoconstriction.…”

Section: Discussionmentioning

confidence: 99%

Neural Network Analysis of the Volumetric Capnogram to Detect Pulmonary Embolism

Patel

Rayburn

Browning

et al. 1999

Chest

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Respiratory Changes in Thromboembolic Disease

Cited by 9 publications

References 11 publications

Inhibition of prostaglandin synthesis during polystyrene microsphere-induced pulmonary embolism in the rat

Inhibition of prostaglandin synthesis during polystyrene microsphere-induced pulmonary embolism in the rat

Value of measurement of alveolo-arterial gradient of PCO2 compared to pulmonary scan in diagnosis of thromboembolic pulmonary disease

Neural Network Analysis of the Volumetric Capnogram to Detect Pulmonary Embolism

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